Mitochondrial inner membrane lipids and proteins as targets for decreasing cardiac ischemia/reperfusion injury

被引:46
作者
Brown, David A. [1 ,3 ]
Sabbah, Hani N. [4 ]
Shaikh, Saame Raza [2 ,3 ]
机构
[1] E Carolina Univ, Brody Sch Med, Dept Physiol, Greenville, NC USA
[2] E Carolina Univ, Brody Sch Med, Dept Biochem & Mol Biol, Greenville, NC USA
[3] E Carolina Univ, Brody Sch Med, East Carolina Diabet & Obes Inst, Greenville, NC USA
[4] Henry Ford Hosp, Dept Internal Med, Detroit, MI 48202 USA
关键词
Cardioprotection; Cardiolipin; Mitochondria; Heart; ACUTE MYOCARDIAL-INFARCTION; CELL-PENETRATING PEPTIDES; FREE-RADICAL GENERATION; COMPLEX-I ACTIVITY; K-ATP CHANNELS; REPERFUSION INJURY; CYTOCHROME-C; N-ACETYLCYSTEINE; RUTHENIUM RED; INDUCED CARDIOPROTECTION;
D O I
10.1016/j.pharmthera.2013.07.005
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
A major manifestation of coronary artery disease is cardiac ischemia/reperfusion injury, with the extent of injury directly relating to short- and long-term prognosis. Emerging evidence suggests that mitochondrial dysfunction is centrally involved in ischemia/reperfusion injury. In this review, we summarize the role of mitochondria in the etiology of ischemia/reperfusion injury. We attempt to highlight emerging areas for cardiac mitochondrial medicine and discuss recent advances regarding the molecular composition of inner membrane channels. We discuss interactions between lipids and proteins in the inner mitochondrial membrane, and the ever-evolving nature of this relationship during ischemia/reperfusion. Potentially novel treatments influencing the biophysical properties of inner membrane lipids (such as cardiolipin) are presented. Finally, we point to areas where future study is needed to expand and improve our understanding of mitochondrial pathophysiology during cardiac ischemia/reperfusion. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:258 / 266
页数:9
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